|Chen, S. - TEXAS A & M|
|Walzem, R. - TEXAS A & M|
Submitted to: Poultry Science Association
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 8, 2005
Publication Date: January 1, 2006
Citation: Chen, S.E., McMurtry, J.P., Walzem, R.L. 2006. Overfeeding-induced ovarian dysfunction in broiler breeder hens is associated with lipotoxicity. Poultry Science. 85.70-81. Interpretive Summary: Genetic selection for rapid growth in modern broiler strains is collaterally associated with specific undesirable traits, including skeletal deformities and metabolic diseases such as ascites, fatty liver and kidney syndrome. In females, the capacity for rapid early growth coupled with free access to feed leads to enhanced adult fatness and poor reproductive performance. These undesirable outcomes appear to arise from increases in feed intake that occurred concomitantly with genetic selection for rapid early growth. In adulthood, persistence of the trait of increased voluntary feed intake results in actual food intakes in excess of the requirement for optimal adult health and performance. These genetic traits impact adult animal health and as a result, nutritional management plays a large role in adult broiler breeder performance. Restriction of feed intake to approximately 50 to 60% of ad libitum feeding is an effective and practical management technique to reduce metabolic disease and improve egg production in broiler breeder hens. Leptin is the best understood of the adipose tissue hormones. Impaired leptin signaling is known to cause increased feed intake, massive obesity, and reproductive failure in mammals. This study was done to test whether lipotoxicity could drive the altered hormonal signals and metabolic homeostasis leading to ovarian dysfunction and reduced egg production in feed satiated broiler breeder hens. The results in the present study strongly indicate that unregulated feed intake and genetic divergence converge to influence reproductive function of broiler breeder hens. These effects appear to be mediated through lipopenic dysregulations and lipotoxic mechanisms. The genetic divergence in the sensitivity of ovarian function in response to feed intake suggests a potential for further improvement in current broiler strains. The results of this study will be of interest to other scientists.
Technical Abstract: Triacylglycerol accumulation in non-adipose tissue, termed lipotoxicity, develops with obesity and can provoke insulin resistance, overt diabetes and ovarian dysfunction. Leptin, an adipose tissue hormone, may mediate these effects. Feed-satiated broiler breeder hens manifest lipotoxicity-like symptoms. Changes in body and organ weights, hepatic and plasma non-esterified fatty acids (NEFA), ovarian morphology, and egg production in response to acute voluntary increases of feed intake in broiler breeder hens were measured in two studies with Cobb 500 broiler breeder hens provided with either 145 or > 290 g feed • hen-1 • day-1 for 10 d. In both studies, no hen fed 145 g feed • day-1 exhibited ovarian abnormalities while ~ 50% of feed-satiated hens did. Egg production in feed-satiated hens was reduced from 73.3 to 55.8% in conjunction with apoptosis-induced atresia of hierarchical follicles. Fractional weight of yolk increased from 29.3 to 30.6% (P < 0.016) and no longer correlated to egg weight. Body, liver and abdominal adipose weights were significantly greater (P < 0.05) in feed-satiated hens, as were plasma concentrations of glucose, NEFA, insulin and leptin (P < 0.05). Feed-satiated hens with abnormal ovaries had significantly more liver and abdominal fat, greater plasma leptin and NEFA concentrations, and more saturated fatty acids in plasma NEFA than feed-satiated hens with normal ovaries. However, these two groups of hens had similar increases in BW gain, NEFA, glucose and insulin concentrations. Leptin mediated lipotoxicity appears to be an upstream event to feed intake associated impaired reproductive performance in broiler breeder hens.